@prefix this: . @prefix sub: . @prefix beldoc: . @prefix rdfs: . @prefix rdf: . @prefix xsd: . @prefix dct: . @prefix dce: . @prefix pav: . @prefix np: . @prefix belv: . @prefix prov: . @prefix chebi: . @prefix sdis: . @prefix obo: . @prefix occursIn: . @prefix species: . @prefix pubmed: . @prefix orcid: . sub:Head { this: np:hasAssertion sub:assertion; np:hasProvenance sub:provenance; np:hasPublicationInfo sub:pubinfo; a np:Nanopublication . } sub:assertion { sub:_1 occursIn: obo:CL_0000312, obo:UBERON_0000014, species:9606; rdf:object sdis:cell%20senescence; rdf:predicate belv:decreases; rdf:subject chebi:9334; a rdf:Statement . sub:assertion rdfs:label "a(CHEBI:sulfasalazine) -| path(SDIS:\"cell senescence\")" . } sub:provenance { beldoc: dce:description "Approximately 61,000 statements."; dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved."; dce:title "BEL Framework Large Corpus Document"; pav:authoredBy sub:_3; pav:version "20131211" . sub:_2 prov:value "To inhibit NF-nB activity, we used sulfasalazine and gliotoxin, two weak inhibitors we have shown previously to delay senescence without inducing massive apoptosis (23). A few days after having treated pre-senescent cells with one of these drugs, emerging clones appeared in 85% of the control wells compared with 50% of those treated by catalase, 0% of the wells with (10 Amol/L) N-tert-butyl-hydroxylamine–treated cells, and 0% of the wells containing NF-nB inhibitors (Fig. 5)."; prov:wasQuotedFrom pubmed:19826058 . sub:_3 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:19826058; prov:wasDerivedFrom beldoc:, sub:_2 . } sub:pubinfo { this: dct:created "2014-07-03T14:33:37.373+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }